Department of Surgery, Maastricht University Medical Centre & Nutrition and Toxicology Research Institute, Maastricht, The Netherlands.
Crit Care Med. 2010 Jan;38(1):133-7. doi: 10.1097/CCM.0b013e3181b4a5ed.
The pathophysiological sequelae of meningococcal sepsis are mainly caused by deregulated microvasculature function, leading to impaired tissue blood flow. Because mature enterocytes are known to be susceptible to altered perfusion, we aimed to investigate: (1) the development of enterocyte damage; and (2) the relation between enterocyte damage and severity of disease and outcome in children with meningococcal sepsis.
Retrospective human study.
Pediatric intensive care unit at a university hospital.
Nineteen consecutive children with meningococcal sepsis were studied during their pediatric intensive care unit stay.
None. MEASUREMENT AND MAIN RESULTS Circulating levels of intestinal fatty acid binding protein, a small cytosolic protein constitutively present in mature enterocytes and released on cell injury, were assessed. Severity of disease was represented by meningococcal-specific Rotterdam Score, generic Pediatric Risk of Mortality II score, and circulating interleukin-6. Clinical outcome was measured by length of pediatric intensive care unit stay and number of ventilator days. Highest plasma intestinal fatty acid binding protein values were measured on pediatric intensive care unit stay admission. At the time of admission, eight of 19 patients had higher intestinal fatty acid binding protein plasma levels than the upper reference limit of 30 healthy volunteers. In all survivors, intestinal fatty acid binding protein levels declined to normal values within 12 hrs after starting intensive treatment, whereas the three nonsurvivors maintained elevated intestinal fatty acid binding protein plasma levels. A significant correlation was found among intestinal fatty acid binding protein and Rotterdam Score, Pediatric Risk of Mortality II, interleukin-6 at admission (Spearman's r = 0.402, p = .006; r = 0.243, p = .045; r = 0.687, p < .001, respectively). Next, a significant correlation was found between intestinal fatty acid binding protein and clinical outcome.
Elevated plasma intestinal fatty acid binding protein is found in eight of 19 children with severe pediatric intensive care unit stay at the time of clinical presentation, suggesting the presence of enterocyte damage. Furthermore, prolonged enterocyte damage is found in nonsurvivors. Further studies are needed to clarify the potential role for assessment of plasma intestinal fatty acid binding protein in monitoring treatment of pediatric intensive care unit stay.
脑膜炎球菌败血症的病理生理后果主要是由于微血管功能失调，导致组织血流受损。由于成熟的肠细胞已知易受灌注改变的影响，我们旨在研究：（1）肠细胞损伤的发展；（2）肠细胞损伤与疾病严重程度和结局的关系在脑膜炎球菌败血症患儿中。
回顾性人体研究。
大学医院儿科重症监护病房。
19 例连续的脑膜炎球菌败血症患儿在儿科重症监护病房住院期间接受研究。
无。
评估循环水平的肠脂肪酸结合蛋白，一种小的胞浆蛋白，在成熟的肠细胞中持续存在，并在细胞损伤时释放。疾病的严重程度由脑膜炎球菌特异性鹿特丹评分、通用儿科死亡率 II 评分和循环白细胞介素-6 来表示。临床结果通过儿科重症监护病房住院时间和呼吸机使用天数来衡量。最高的血浆肠脂肪酸结合蛋白值在儿科重症监护病房住院期间测量。在入院时，19 例患者中有 8 例的肠脂肪酸结合蛋白血浆水平高于 30 名健康志愿者的参考上限。在所有幸存者中，肠脂肪酸结合蛋白水平在开始强化治疗后 12 小时内降至正常水平，而 3 例非幸存者则维持升高的肠脂肪酸结合蛋白血浆水平。在入院时，肠脂肪酸结合蛋白与鹿特丹评分、儿科死亡率 II、白细胞介素-6 之间存在显著相关性（Spearman's r = 0.402，p =.006；r = 0.243，p =.045；r = 0.687，p <.001）。其次，肠脂肪酸结合蛋白与临床结果之间存在显著相关性。
在 19 例需要入住儿科重症监护病房的严重患儿中，有 8 例患儿在临床出现时发现血浆肠脂肪酸结合蛋白升高，提示存在肠细胞损伤。此外，在幸存者中发现了延长的肠细胞损伤。需要进一步研究以阐明评估血浆肠脂肪酸结合蛋白在监测儿科重症监护病房治疗中的潜在作用。
